Harmful Algal Blooms (HABs) are attributable to rapid, localized growth of “algae” and other species, most of which are photosynthetic. There is evidence to indicate that HABs are occurring with increasing frequency, probably because of the combined effects of a number of factors, including changes in nutrient addition, introduction or seeding of non-indigenous species, and climate change (e.g., Heisler et al., (2008) Harmful Algae. 8: 3-13 (2016). The cyanobacteria that are responsible for HAB events generate metabolic products called cyanotoxins that express toxicity, usually toward digestive organs (e.g., liver, kidney) or the central nervous system.
Microcystin (MC) contamination has become a worldwide concern because of the increased occurrence of cyanobacteria blooms in surface waters that are used for drinking water supplies (Bogialli et al., (2006) Environ. Sci. Technol. 40: 2917-2923; Westrick et al., (2010) Anal. Bioanal. Chem. 397: 1705-1714; Zamyadi et al., (2012) Water Res. 46: 1511-1523). MCs are potent hepatotoxins that comprise a group of cyclic heptapeptides containing a relatively large amino acid moiety (Adda) and two variable amino acid moieties (He et al., (2012) Water Res. 46: 1501-1510). One of the most widespread and toxic MCs is microcystin-LR (MC-LR), the variable amino acids of which are leucine and arginine, accounting for 46.0%-99.8% of the total MCs in cyanobacterial blooms (Zong et al., (2013) J. Hazard. Mater. 252, 293-299; Sharma et al., (2012) Sep. Purif. Technol. 91, 3-17).
MC-LR has been shown to induce chronic or acute liver injury by inhibiting activity of protein phosphatases 1 and 2A (Campos et al., (2010) Int. J. Mol. Sci. 11: 268-287; Herfindal & Selheim (2006) Med Chem. 6: 279-285). MC-LR has also been identified as a tumor initiator and promoter in human liver and colorectal cells (Eriksson et al., (1990) Biochem. Biophys. Res. Commun. 173: 1347-1353; Hooser, S. B., (2000) Toxicol. Pathol. 28: 726-733). The World Health Organization has proposed a provisional guideline concentration of 1.0 μg/L for MC-LR (free plus cell-bound) in drinking water (Guidelines for drinking-water quality: recommendations. World Health Organization: (2004) Vol. 1).
Previous studies have indicated that chlorination can be applied for MC degradation (Tsuji et al., (1997) Toxicon 35: 1033-1041). The apparent second-order rate constant for chlorination of MC-LR at 20:1 chlorine:MC-LR molar ratio and 20° C. has been reported as 127.8 M−1 s−1 at pH 6.1, 91.5 M−1 s−1 at pH 7, and 33.1 M−1 s−1 at pH 8 (Acero et al., (2005) Water Res. 39: 1628-1638). These observations suggested that hypochlorous acid is the main active species in MC-LR chlorination. However, high chlorine doses and long contact times are required in this process, leading to the formation of suspected carcinogenic byproducts (Zong et al., (2013) J. Hazard. Mater. 252, 293-299).
It also has been reported that MC-LR undergoes photolysis upon exposure to germicidal ultraviolet (UV) radiation (Tsuji et al., (1995) Toxicon 33: 1619-1631). However, UV doses required for MC-LR photodecomposition range from 1,530 mJ/cm2 to 20,000 mJ/cm2, roughly 1-3 orders of magnitude greater than those required for disinfection (Hijnen et al., (2006) Water Res. 40: 3-22).
A high-profile example of MC-LR contamination occurred in Toledo (OH, U.S.) in 2014. The Toledo water supply was shut down for several days because the MC concentration in their finished water supply was unacceptably high. It should be noted that the Toledo water supply is disinfected using chlorine. However, chlorination was not able to reduce the MC concentration to a point that conformed to WHO Guidelines. Therefore, an ongoing need exists to develop more effective processes for MC control.
Advanced oxidation processes (AOPs) have been investigated for degradation of MC-LR by hydroxyl radicals. For perspective, the rate constant for the reaction between hydroxyl radicals and MC-LR has been reported to be 2.3 (±0.1)×1010 M−1 s−1 (Song et al., (2009) Environ. Sci. Technol. 43: 1487-1492). This reaction is sufficiently fast that it may be considered to be a diffusion-controlled process. The combined application of chlorination and UV irradiation is often described as an AOP, involving the generation of oxidizing radicals (Sichel et al., (2011) Water Res. 45: 6371-6380; Watts & Linden (2007) Water Res. 41: 2871-2878). However, no information is available to describe the effects of combined chlorine/UV process for MC-LR decomposition.
This conventional view of the chlorine/UV process as an AOP has focused on photolysis of free chorine to yield a hydroxyl radical and a chlorine free radical (Feng et al., (2007) J. Environ. Eng. Sci. 6: 277-284). These radicals can contribute to decomposition of target compounds. However, another pathway may exist whereby chlorine and UV radiation may act synergistically to degrade target compounds. It has been demonstrated that chlorination of amines will activate these compounds toward UV photodegradation (Zhang et al., (2015) Water Res. 68, 804-811; Li & Blatchley III, (2009) Environ. Sci. Technol. 43: 60-65; Weng & Blatchley III (2013) Environ. Sci. Technol. 47: 4269-4276; Weng et al., (2012) Water Res. 46: 2674-2682). Chlorinated amines generally have higher molar absorptivity (ε254) and quantum yield (Φ254) than their respective unchlorinated parent compounds. As an example, ε254 and Φ254 for photodegradation of creatinine have been reported to be 1293 M−1·cm−1 and 0.011±0.002 mol/E, respectively, whereas corresponding values of N-chloro-creatinine increased to 3911 M−1·cm−1 and 0.144±0.011 mol/E (Weng et al., (2013) Water Res. 47: 4948-4956).